You must be logged in to access this feature.

The technical and physiologic aspects of mechanical ventilation during surgery have not changed for decades. For example, the use of positive-pressure ventilation during general anesthesia causes a maldistribution of inspired gas relative to pulmonary perfusion. As a result, alveolar dead space increases, and supplemental oxygen must be given to prevent hypoxemia resulting from areas of lung with a low ventilation-to-perfusion ratio. More often than not, relative overventilation causes hypocapnic alkalosis. Ideally, mechanical ventilation instituted during general anesthesia would provide adequate alveolar ventilation with a minimal increase in airway pressure and a minimal displacement of the operative site. The traditional method of producing ventilation for general anesthesia, controlled mechanical ventilation (CMV), consists of intermittent delivery of a selected tidal volume (VT) with an attendant peak airway pressure of 15 - 30 cm H2O. Based on our experience with alternate ventilatory modes in critically ill patients, we designed a means to produce ventilatory support for anesthetized patients.

Airway pressure-release ventilation (APRV) has been used successfully to ventilate anesthetized animals [1–3] and unanesthetized humans. [4–7] During APRV, continuous positive airway pressure (CPAP) is titrated to an optimal level. Airway pressure is then decreased intermittently. Gas exists the lungs and lung volume decreases, allowing excretion of carbon dioxide. After a selected release time, airway pressure and lung volume are rapidly reestablished. Spontaneous breathing is possible at any time.

Because most reports have indicated that APRV can augment ventilation with peak airway pressure and improved efficiency compared with traditional modes of positive pressure ventilation, [1,2,4,6,8] we designed a similar ventilatory pattern for use in anesthetized patients, intermittent continuous positive airway pressure (CPAPI). We had two goals:(1) to compare the efficiency of ventilation during CMV with that during CPAPI in patients undergoing general anesthesia and intraabdominal operations and (2) to test the hypothesis that the partial pressure of end-tidal carbon dioxide (PETCO2) is a more accurate reflection of the partial pressure of arterial carbon dioxide (PaCO2) during CPAPI than during CMV.

Materials and Methods

We studied patients classified as physical status 1 and 2 of the American Society of Anesthesiologists who were scheduled for general anesthesia, intraabdominal operation, and insertion of an intraarterial catheter to monitor blood pressure. All patients signed a consent form approved by the Institutional Review Board. Excluded were patients who had unstable cardiovascular function or severe obstructive lung disease. Chest leads II and V5 were attached for electrocardiographic monitoring, and heart rate was determined electronically. A probe placed on a finger tip allowed oxygen saturation to be measured by pulse oximetry.

Anesthesia and neuromuscular blockade were induced with propofol (1 or 2 mg/kg administered intravenously), or thiopental (2–5 mg/kg administered intravenously) and succinylcholine (1.5 mg/kg administered intravenously), respectively. Anesthesia and neuromuscular blockade were maintained with isoflurane, nitrous oxide, and oxygen or with vecuronium, respectively. All patients were orotracheally intubated. Patients initially were ventilated with CMV using a VT of 8–10 ml/kg and a respiratory rate sufficient to keep PETCO2between 30 and 35 mmHg. The fractional concentration of inspired oxygen (FIO2) was adjusted to keep the Sp (O)2at 90% or higher. A thermistor placed in the esophagus monitored temperature. A catheter inserted into the radial artery permitted determination of blood pressure, pHa, PaCO2, PaO2, hemoglobin concentration, and oxyhemoglobin saturation. A flow transducer (VarFlex; Allied Healthcare Products, Irvine, CA) attached to the tracheal tube was connected to a pulmonary mechanics computer (BICORE CP-100; Allied Healthcare Products) to determine VT, respiratory rate, minute ventilation (VE), peak inspiratory gas flow rate, and peak and mean airway pressures. The pulmonary mechanics monitor is factory calibrated with room air (oral communication, Larry Butcher, Allied Healthcare Engineering Department, 1996), so that volumes calculated during general anesthesia necessitated correction for nitrous oxide and isoflurane. Using a calibrated 1–1 super syringe (Hamilton Medical Corp., Reno, NV), identical volumes of room air and a gas mixture identical to that breathed by the patient were injected through the pneumotachograph. The resulting ratio (volume air:volume anesthetic gas mixture) was used to correct the respired gas volumes obtained from the computer during the investigation. The sample tubing of a gas and anesthetic vapor monitor (Ultima; Datex-Engstrom, Helsinki, Finland) was positioned between the pneumotachograph and the anesthesia breathing circuit to determine the fractional concentration of inspired oxygen, PETCO2, and the end-tidal concentrations of isoflurane and nitrous oxide. Baseline data were collected after the abdominal incision was made, and heart rate, mean arterial blood pressure, and end-expired concentration of isoflurane remained unchanged for 30 min. We assumed relatively constant PaCO2and carbon dioxide production, and we quantified the efficiency of ventilation by calculating PaCO2/VE(the normal value is approximately 7.4 mmHg [middle dot] 1-1[middle dot] min-1for awake humans).

Patients were assigned randomly to receive alternating 20-min trials of CMV (using the same characteristics as baseline) and CPAPI. To provide CPAPI, we used a modified ventilator (model Mark 4A; Bird Corp., Palm Springs, CA). Alveolar ventilation is produced by intermittent release of CPAP nearly to atmospheric pressure (Figure 1). After a release period is 1 s, CPAP is restored and lung volume is reestablished. The respiratory rate during CPAPI was the same as during baseline CMV. However, because previous investigations revealed that dead-space ventilation was lower during APRV than during CMV, during CPAPI [1,6] the desired tidal volume was obtained by titration of CPAP to produce a PETCO2that was 2 or 3 mmHg more than the value observed during baseline CMV; this was performed to try to produce equivalent alveolar ventilation and PaCO2.

Figure 1. Changes in airway pressure and lung volume during controlled mechanical ventilation (CMV) and during intermittent continuous positive airway pressure (CPAPI). During CMV, airway pressure increases from ambient, and the peak pressure usually ranges from 15 to 30 cm H2O in anesthetized patients. In contrast, pressure is released from a selected level of CPAP during CPAPI. During CMV, lung volume increases from the functional residual capacity. In contrast, lung volume decreases from an elevated baseline value during CPAPI. After a selected release time, lung volume is reestablished rapidly by reapplication of CPAP.

Figure 1. Changes in airway pressure and lung volume during controlled mechanical ventilation (CMV) and during intermittent continuous positive airway pressure (CPAPI). During CMV, airway pressure increases from ambient, and the peak pressure usually ranges from 15 to 30 cm H2O in anesthetized patients. In contrast, pressure is released from a selected level of CPAP during CPAPI. During CMV, lung volume increases from the functional residual capacity. In contrast, lung volume decreases from an elevated baseline value during CPAPI. After a selected release time, lung volume is reestablished rapidly by reapplication of CPAP.

Data are summarized as mean +/- 1 SD. To assess the possibility of a carry over of treatment effect (treatment - period interaction), we compared the differences (mean +/- 1 SD) for the two treatment sequences. [9] To compare the differences between the two treatment sequences, we applied the Student's t test for independent observations. There was no significant treatment - period interaction, therefore, data were compared statistically using the Student's t test for paired observations (two tailed). We used regression analysis to assess the mathematical relation between PETCO2and PaCO2. We tested the null hypothesis that the two regressions were coincident (i.e., they have the same slope and intercept) according to the technique described by Glantz. [10] We also quantified the strength of the association between PETCO2and Pa (CO)2by calculating Pearson's product-moment correlation (r). We tested the null hypothesis that the two correlations were the same according to a technique described by Zar. [11]

Results

Twenty patients (11 women, 9 men) who were 62 +/- 15 yr old and who weighed 88 +/- 26 kg underwent similar anesthesia care and operative procedures. The end-tidal concentration of isoflurane (1.1 +/- 0.3%), body temperature (35.7%+/- 0.5 [degree sign]C), and hemoglobin concentration (10.8 +/- 1.5 g/dl) were similar throughout the study, and intertrial data were pooled for summary. There were no differences in variables reflecting cardio-vascular function throughout the study (Table 1).

Peak airway pressure was less during CPAPI than during CMV (Table 2). During CPAPI, peak airway pressure did not exceed 18 cm H2O in any patient, and in six patients, it was less than one half that observed during CMV. Although mean airway pressure was higher during CPAPI, no adverse cardiovascular consequences were apparent. During CMV, peak inspiratory gas flow rate was 0.7 +/- 0.2 1/min. After interruption of CPAP during CPAPI, a peak flow of 1.3 +/- 0.4 l/min restored the CPAP level. The respiratory rate was similar by design, but during CPAPI, comparable PaCO2was achieved with less tidal volume and minute ventilation. Thus CPAPI improved the efficiency of ventilation, as quantified by a higher value for PaCO(2/VE)(Table 3).

There were no differences in the fractional concentration of inspired oxygen, and arterial blood gas tensions, pHa, and oxyhemoglobin saturation did not change during the study. The correlation coefficient between PaCO2and PETCO2was closer to unity for CPAPI (r = 0.95) than for CMV (r = 0.80; P < 0.10;Figure 2). There was a significant difference in the lines of least squares resulting from the regression of PETCO2on PaCO2during CMV versus CPAPI (P < 0.001). The slope of the regression ([small beta, Greek]) of PETCO2on PaCO2was closer to 1 during CPAPI ([small beta, Greek]= 0.90) than during CMV ([small beta, Greek]= 0.62). The y-axis intercept ([small alpha, Greek]) was 2.43 during CPAPI and 9.07 during CMV. The arterial-to-end-tidal carbon dioxide partial pressure difference [P(a - ET)CO2] was always less during CPAPI (1.7 +/- 0.9 mmHg) than during CMV (6.3 +/- 1.6 mmHg; P < 0.0001) and was never more than 3.5 mmHg during CPAPI. During CMV, P(a - ET)CO2ranged from 4 to 10 mmHg.

Figure 2. The relation between end-tidal carbon dioxide tension (PETCO(2)) versus the partial pressure of arterial carbon dioxide (PaCO2) in 20 patients who received alternate trials of intermittent continuous positive airway pressure (CPAP; solid circles) and controlled mechanical ventilation (open circles). The line of identity (dotted) and a mathematically determined line of best fit (solid) associated with each data cloud were plotted. Regression equations for the line of best fit during CPAPI and CMV were PETCO2= 2.4 mmHg + 0.9 x PaCO2and PETCO2= 9.1 mmHg + 0.6 x PaCO2, respectively. *P < 0.001 using a technique described by Zar. [11]

Figure 2. The relation between end-tidal carbon dioxide tension (PETCO(2)) versus the partial pressure of arterial carbon dioxide (PaCO2) in 20 patients who received alternate trials of intermittent continuous positive airway pressure (CPAP; solid circles) and controlled mechanical ventilation (open circles). The line of identity (dotted) and a mathematically determined line of best fit (solid) associated with each data cloud were plotted. Regression equations for the line of best fit during CPAPI and CMV were PETCO2= 2.4 mmHg + 0.9 x PaCO2and PETCO2= 9.1 mmHg + 0.6 x PaCO2, respectively. *P < 0.001 using a technique described by Zar. [11]

We designed and tried to evaluate CPAPI as a ventilatory support technique for patients undergoing general anesthesia and neuromuscular blockade. We observed that the minute ventilation necessary to achieve similar alveolar ventilation, as reflected by PaCO2, was less when patients were ventilated with CPAPI versus CMV. Normal awake VT is approximately 6 ml/kg. Our results indicate that such a VT provided by CPAPI at a rate of 7/min will produce a normal PaCO2. Because anatomic dead space was presumed to be nearly constant, the ability to achieve comparable PaCO2with a lower P(a - ET)CO2and a lesser minute ventilation was evidence of less alveolar dead-space ventilation during CPAPI. The reduction in alveolar dead space ventilation rendered PET (CO)2a more accurate reflection of PaCO2during CPAPI than during CMV. The observation that dead-space ventilation is lower also has been commonly noted during APRV. This finding may be explained by the similarly low peak airway pressure during CPAPI and APRV. [1,2,6] Although mean airway pressure was higher during our trials of CPAPI, no adverse cardiovascular consequences seemed to occur.

The following Equation providesan estimate of the amount of change (Delta) in functional residual capacity (FRC) effected by CPAP:

Airway pressure - release ventilation provides adequate alveolar ventilation in anesthetized experimental animals with healthy and injured lungs and in patients with mild to severe acute lung injury. Fundamentally, APRV differs from other methods of positive pressure ventilation in that it is a CPAP system designed to increase resting lung volume and to augment alveolar ventilation, when spontaneous ventilation is inadequate. Several factors determine the VT produced by APRV: release time, release pressure, airway resistance, and lung-thorax compliance. The time necessary for gas to leave the lung during pressure release is determined by CLT and the resistance to gas flow. The product of these variables is the time constant for exhalation, and, as long as the release time exceeds three time constants, the VT is the product of CLT and the release pressure. [4] Because all of these principles also apply to CPAPI, it may be possible to monitor respiratory mechanics continuously during CPAPI in anesthetized patients.

Positive-pressure inflation of the lungs can cause adverse cardiovascular effects. We found no differences in cardiovascular function during CPAPI and CMV, which probably was caused by the low mean airway pressure observed with both modes. Previous investigations have reported adverse cardiovascular sequelae that occurred with intermittent positive-pressure ventilation, but not with APRV. [1,2] Because APRV provides mechanical ventilation by decreasing airway pressure from a level of CPAP titrated to optimize lung mechanics, peak airway pressure never exceeds CPAP, and mean airway pressure is less than the CPAP level. Therefore, the lack of adverse pressure-related effects is not surprising.

The value for P(a - ET)CO2during CPAPI was similar to that observed in spontaneously breathing patients. [14] During spontaneous breathing, inspired gas is distributed predominately to relatively well-perfused alveoli in dependent lung regions, and the end-expired gas closely approximates alveolar gas. However, in anesthetized, paralyzed, and mechanically ventilated patients, the inspired gas is distributed preferentially to poorly perfused or nonperfused alveoli in nondependent lung units, and the end-expired gas contains a significant contribution from alveolar dead space. [15–18] During normal spontaneous breathing, P(a - ET)CO2may range from 1 to 3 mmHg. [14] During CMV, P(a - ET)(CO)2may exceed 12 mmHg and is rarely < 6 mmHg. [18] When mechanical inspiration occurs from a lung volume less than normal FRC, the maldistribution of inspired air relative to perfusion is exaggerated. [19] Thus, alveolar dead-space ventilation is greater during CMV, particularly when FRC decreases, as occurs immediately after induction of general anesthesia.

Valentine et al. [6] observed a distribution of less ventilation to nonperfused alveoli (dead space) with similar tidal volume and frequency during APRV than during intermittent mandatory ventilation and pressure support ventilation. Although we did not quantify dead space, the improved efficiency of ventilation during CPAPI versus CMV, as evidenced by a higher value for PaCO2/VE, indicates that alveolar dead-space ventilation was less during CPAPI. As noted in Figure 2, the slope and intercept of the least-squares regression lines for PETCO2versus PaCO2are different for CMV and CPAPI. Furthermore, the slope of the least-squares regression line for PETCO2versus PaCO2obtained during CPAPI was 0.90 and the y-axis intercept was 2.43 mmHg, indicating that PETCO2closely reflects PaCO2, regardless of the PaCO2value. In contrast, with higher values of PaCO(2) observed during CMV, P(a - ET)CO2increased, secondary to increased alveolar dead space, rendering PETCO2a progressively less accurate monitor of PaCO2. Presumably, lower peak airway pressure during CPAPI caused less alveolar dead space in nondependent lung regions.

Intermittent CPAP; pressure-controlled, inverse ratio ventilation; and APRV share several common characteristics, but conceptually they are quite different. Pressure-controlled, inverse ratio ventilation is applied to critically ill patients with severe respiratory dysfunction, usually with an elevated end-expiratory pressure. Spontaneous breathing is not possible and extreme sedation, muscle relaxation, or both, usually are administered. A pressure limit is selected to produce acceptable VT and peak positive airway pressures. As the patient's condition improves, pressure-controlled, inverse ratio ventilation gradually is discontinued by decreasing inspiratory time and mean positive airway pressure.

Airway pressure - release ventilation is applied to spontaneously breathing patients with a restrictive ventilatory defect to optimize FRC with CPAP. If necessary, the CPAP level is decreased briefly (usually 1 s or less) to allow a decrease in lung volume and carbon dioxide excretion. As the patient's condition improves, and he or she is more able to breathe, the rate of release is decreased and mean airway pressure increases.

During general anesthesia, CPAPI is applied to a level that will produce a desirable VT when removed. Then the CPAP is reduced intermittently to produce ventilation; there is no intent to “restore” normal FRC, to optimize lung mechanics, or to improve oxygenation. Then, CPAPI can be discontinued at the end of the anesthetic. Although the airway pressure patterns may be similar, pressure-controlled, inverse ratio ventilation; APRV; and CPAPI are distinctly different in concept, application, and mode of discontinuation.

Because our patients received continuous neuromuscular blockade, CMV and CPAPI both provided total ventilatory support. Existing methods do not permit application of partial ventilatory support techniques, such as intermittent mandatory ventilation or APRV, during anesthesia. However, the use of CPAPI to provide partial mechanical support of spontaneously breathing patients who cannot maintain an acceptable PaCO2during general anesthesia may have several advantages over the use of CMV:(1) lower mean intrathoracic (pleural) pressure;(2) augmented venous return and improved cardiovascular performance; and (3) better distribution of inspired gas, resulting in improved matching of ventilation and perfusion. All of these advantages occur when APRV is used to provide partial ventilatory support in awake humans. [8] The role for CPAPI in partial ventilatory support during general anesthesia should be evaluated.

Our results indicate that CPAPI provides more efficient ventilation of patients undergoing general anesthesia, with a significantly lower peak airway pressure compared with CMV. An improved efficiency of ventilation decreases the necessary minute ventilation and permits reduction of VT, respiratory rate, or both, thus reducing the magnitude or frequency, respectively, of lung inflation. Thus, there is less respiratory movement and possible improvement in technical conditions during intraabdominal operations. During CPAPI, P(a - ET)CO2approximates the value observed during spontaneous breathing, rendering PETCO2a more accurate monitor of ventilation during CPAPI than during CMV.

Intermittent CPAP is a unique way to provide ventilatory support to anesthetized patients. It may have significant advantages with regard to gas exchange, efficiency of ventilation, and hemodynamic stability. Future investigations will determine the usefulness of CPAPI in clinical practice.

Figure 1. Changes in airway pressure and lung volume during controlled mechanical ventilation (CMV) and during intermittent continuous positive airway pressure (CPAPI). During CMV, airway pressure increases from ambient, and the peak pressure usually ranges from 15 to 30 cm H2O in anesthetized patients. In contrast, pressure is released from a selected level of CPAP during CPAPI. During CMV, lung volume increases from the functional residual capacity. In contrast, lung volume decreases from an elevated baseline value during CPAPI. After a selected release time, lung volume is reestablished rapidly by reapplication of CPAP.

Figure 1. Changes in airway pressure and lung volume during controlled mechanical ventilation (CMV) and during intermittent continuous positive airway pressure (CPAPI). During CMV, airway pressure increases from ambient, and the peak pressure usually ranges from 15 to 30 cm H2O in anesthetized patients. In contrast, pressure is released from a selected level of CPAP during CPAPI. During CMV, lung volume increases from the functional residual capacity. In contrast, lung volume decreases from an elevated baseline value during CPAPI. After a selected release time, lung volume is reestablished rapidly by reapplication of CPAP.

Figure 2. The relation between end-tidal carbon dioxide tension (PETCO(2)) versus the partial pressure of arterial carbon dioxide (PaCO2) in 20 patients who received alternate trials of intermittent continuous positive airway pressure (CPAP; solid circles) and controlled mechanical ventilation (open circles). The line of identity (dotted) and a mathematically determined line of best fit (solid) associated with each data cloud were plotted. Regression equations for the line of best fit during CPAPI and CMV were PETCO2= 2.4 mmHg + 0.9 x PaCO2and PETCO2= 9.1 mmHg + 0.6 x PaCO2, respectively. *P < 0.001 using a technique described by Zar. [11]

Figure 2. The relation between end-tidal carbon dioxide tension (PETCO(2)) versus the partial pressure of arterial carbon dioxide (PaCO2) in 20 patients who received alternate trials of intermittent continuous positive airway pressure (CPAP; solid circles) and controlled mechanical ventilation (open circles). The line of identity (dotted) and a mathematically determined line of best fit (solid) associated with each data cloud were plotted. Regression equations for the line of best fit during CPAPI and CMV were PETCO2= 2.4 mmHg + 0.9 x PaCO2and PETCO2= 9.1 mmHg + 0.6 x PaCO2, respectively. *P < 0.001 using a technique described by Zar. [11]